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Biomedicines
Special Issues
Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases
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Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 11815

Special Issue Editor

Dr. Renato Socodato

E-Mail Website
Guest Editor
Glial Cell Biology Group, Instituto de Investigação e Inovação em Saúde (i3S), Instituto de Biologia Molecular e Celular (IBMC), University of Porto, 4200-135 Porto, Portugal
Interests: microglia; RhoGTPases; synaptic plasticity; neurodegeneration; cytoskeleton; redox balance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The realization that glial dysfunction plays a causative role in neurological conditions, including major neurodegenerative disorders such Alzheimer's disease, Parkinson´s disease, multiple sclerosis and others, dramatically changed the way that we look at the brain. From this perspective, neuron-glia communication takes center stage, and elucidating the nature of glial dysfunction and the impairment of neuron-glia crosstalk became an urgent, necessary and timely task. This knowledge will most likely provide us with new fundamental insight into brain function mechanisms that may help in treating brain diseases. This Special Issue of Biomedicines is open to articles, in any format, that provide deeper and novel mechanistic insights into the dysregulation of glial function in different neurologiacal conditions, as well as the elucidation of how glial dysfunction can impair neuronal homeostasis and plasticity in brain diseases.

Dr. Renato Socodato
Guest Editor

Manuscript Submission Information

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Keywords

  • glial cell
  • neurodegenerative disorder
  • neuron-glia communication
  • neuronal homeostasis
  • plasticity

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Published Papers (5 papers)

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Research

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14 pages, 3787 KiB  
Article
The Effects of the S1P Receptor Agonist Fingolimod (FTY720) on Central and Peripheral Myelin in Twitcher Mice
by Sibylle Béchet and Kumlesh K. Dev
Biomedicines 2024, 12(3), 594; https://doi.org/10.3390/biomedicines12030594 - 6 Mar 2024
Viewed by 970
Abstract
Krabbe’s disease (KD) is caused by mutations in the lysosomal enzyme galactocerebrosidase and is associated with psychosine toxicity. The sphingosine 1-phosphate receptor (S1PR) agonist fingolimod (FTY720) attenuates psychosine-induced cell death of human astrocytes, demyelination in cerebellar slices, as well as demyelination in the [...] Read more.
Krabbe’s disease (KD) is caused by mutations in the lysosomal enzyme galactocerebrosidase and is associated with psychosine toxicity. The sphingosine 1-phosphate receptor (S1PR) agonist fingolimod (FTY720) attenuates psychosine-induced cell death of human astrocytes, demyelination in cerebellar slices, as well as demyelination in the central nervous system of twitcher mice. Psychosine also accumulates in the peripheral nervous system in twitcher mice; however, effects of fingolimod on this peripheral myelin have not been examined. The aim of this study was to investigate the effects of fingolimod administration on peripheral and central markers of myelination. Here, we report that fingolimod administration (1 mg/kg/day) from postnatal day 5 (PND) onwards did not alter peripheral demyelination in the sciatic nerve of twitcher mice, despite significantly reducing myelin debris, glial reactivity, and neuronal damage in the cerebellum. We also find fingolimod administration improves twitching and mobility scores in twitcher mice. Importantly, we find that fingolimod significantly increases the lifespan of twitcher mice by approximately 5 days. These findings suggest differential effects of fingolimod on peripheral and central neuropathy in twitcher mice, which may explain its modest efficacy on behavior and lifespan. Full article
(This article belongs to the Special Issue Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases)
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19 pages, 2964 KiB  
Article
Insights into the Potential Impact of Quetiapine on the Microglial Trajectory and Inflammatory Response in Organotypic Cortical Cultures Derived from Rat Offspring
by Katarzyna Chamera, Katarzyna Curzytek, Kinga Kamińska, Ewa Trojan, Monika Leśkiewicz, Kinga Tylek, Magdalena Regulska and Agnieszka Basta-Kaim
Biomedicines 2023, 11(5), 1405; https://doi.org/10.3390/biomedicines11051405 - 9 May 2023
Cited by 1 | Viewed by 1819
Abstract
Atypical antipsychotics currently constitute the first-line medication for schizophrenia, with quetiapine being one of the most commonly prescribed representatives of the group. Along with its specific affinity for multiple receptors, this compound exerts other biological characteristics, among which anti-inflammatory effects are strongly suggested. [...] Read more.
Atypical antipsychotics currently constitute the first-line medication for schizophrenia, with quetiapine being one of the most commonly prescribed representatives of the group. Along with its specific affinity for multiple receptors, this compound exerts other biological characteristics, among which anti-inflammatory effects are strongly suggested. Simultaneously, published data indicated that inflammation and microglial activation could be diminished by stimulation of the CD200 receptor (CD200R), which takes place by binding to its ligand (CD200) or soluble CD200 fusion protein (CD200Fc). Therefore, in the present study, we sought to evaluate whether quetiapine could affect certain aspects of microglial activity, including the CD200-CD200R and CX3CL1-CX3CR1 axes, which are involved in the regulation of neuron–microglia interactions, as well as the expression of selected markers of the pro- and anti-inflammatory profile of microglia (Cd40, Il-1β, Il-6, Cebpb, Cd206, Arg1, Il-10 and Tgf-β). Concurrently, we examined the impact of quetiapine and CD200Fc on the IL-6 and IL-10 protein levels. The abovementioned aspects were investigated in organotypic cortical cultures (OCCs) prepared from the offspring of control rats (control OCCs) or those subjected to maternal immune activation (MIA OCCs), which is a widely implemented approach to explore schizophrenia-like disturbances in animals. The experiments were performed under basal conditions and after additional exposure to the bacterial endotoxin lipopolysaccharide (LPS), according to the “two-hit” hypothesis of schizophrenia. The results of our research revealed differences between control and MIA OCCs under basal conditions and in response to treatment with LPS in terms of lactate dehydrogenase and nitric oxide release as well as Cd200r, Il-1β, Il-6 and Cd206 expression. The additional stimulation with the bacterial endotoxin resulted in a notable change in the mRNA levels of pro- and anti-inflammatory microglial markers in both types of OCCs. Quetiapine diminished the influence of LPS on Il-1β, Il-6, Cebpb and Arg1 expression in control OCCs as well as on IL-6 and IL-10 levels in MIA OCCs. Moreover, CD200Fc reduced the impact of the bacterial endotoxin on IL-6 production in MIA OCCs. Thus, our results demonstrated that quetiapine, as well as the stimulation of CD200R by CD200Fc, beneficially affected LPS-induced neuroimmunological changes, including microglia-related activation. Full article
(This article belongs to the Special Issue Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases)
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13 pages, 5668 KiB  
Article
Low Temperature Delays the Effects of Ischemia in Bergmann Glia and in Cerebellar Tissue Swelling
by Xia Li, Romain Helleringer, Lora L. Martucci, Glenn Dallérac, José-Manuel Cancela and Micaela Galante
Biomedicines 2023, 11(5), 1363; https://doi.org/10.3390/biomedicines11051363 - 5 May 2023
Viewed by 1451
Abstract
Cerebral ischemia results in oxygen and glucose deprivation that most commonly occurs after a reduction or interruption in the blood supply to the brain. The consequences of cerebral ischemia are complex and involve the loss of metabolic ATP, excessive K+ and glutamate [...] Read more.
Cerebral ischemia results in oxygen and glucose deprivation that most commonly occurs after a reduction or interruption in the blood supply to the brain. The consequences of cerebral ischemia are complex and involve the loss of metabolic ATP, excessive K+ and glutamate accumulation in the extracellular space, electrolyte imbalance, and brain edema formation. So far, several treatments have been proposed to alleviate ischemic damage, yet few are effective. Here, we focused on the neuroprotective role of lowering the temperature in ischemia mimicked by an episode of oxygen and glucose deprivation (OGD) in mouse cerebellar slices. Our results suggest that lowering the temperature of the extracellular ‘milieu’ delays both the increases in [K+]e and tissue swelling, two dreaded consequences of cerebellar ischemia. Moreover, radial glial cells (Bergmann glia) display morphological changes and membrane depolarizations that are markedly impeded by lowering the temperature. Overall, in this model of cerebellar ischemia, hypothermia reduces the deleterious homeostatic changes regulated by Bergmann glia. Full article
(This article belongs to the Special Issue Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases)
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21 pages, 3276 KiB  
Article
NO-Dependent Mechanisms of p53 Expression and Cell Death in Rat’s Dorsal Root Ganglia after Sciatic-Nerve Transection
by Stanislav Rodkin, Valentina Dzreyan, Mikhail Bibov, Alexey Ermakov, Tatyana Derezina and Evgeniya Kirichenko
Biomedicines 2022, 10(7), 1664; https://doi.org/10.3390/biomedicines10071664 - 11 Jul 2022
Cited by 5 | Viewed by 3590
Abstract
Peripheral-nerve injury is a frequent cause of disability. Presently, no clinically effective neuroprotectors have been found. We have studied the NO-dependent expression of p53 in the neurons and glial cells of the dorsal root ganglia (DRG) of a rat’s spinal cord, as well [...] Read more.
Peripheral-nerve injury is a frequent cause of disability. Presently, no clinically effective neuroprotectors have been found. We have studied the NO-dependent expression of p53 in the neurons and glial cells of the dorsal root ganglia (DRG) of a rat’s spinal cord, as well as the role of NO in the death of these cells under the conditions of axonal stress, using sciatic-nerve axotomy as a model. It was found out that axotomy led to the nuclear–cytoplasmic redistribution of p53 in neurons, 24 h after trauma. The NO donor led to a considerable increase in the level of p53 in nuclei and, to a smaller degree, in the cytoplasm of neurons and karyoplasm of glial cells 4 and 24 h after axotomy. Application of a selective inhibitor of inducible NO-synthase (iNOS) provided the opposite effect. Introduction of the NO donor resulted in a significant increase in cell death in the injured ipsilateral DRG, 24 h and 7 days after trauma. The selective inhibitor of iNOS demonstrated a neuroprotective effect. Axotomy was shown to upregulate the iNOS in nuclei and cytoplasm of DRG cells. The NO-dependent expression of p53, which is particularly achieved through iNOS activation, is believed to be a putative signaling mechanism of neural and glial-cell death after axotomy. Full article
(This article belongs to the Special Issue Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases)
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Review

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11 pages, 647 KiB  
Review
Liver X Receptor Regulation of Glial Cell Functions in the CNS
by Xiaoyu Song, Wanfu Wu, Margaret Warner and Jan-Åke Gustafsson
Biomedicines 2022, 10(9), 2165; https://doi.org/10.3390/biomedicines10092165 - 2 Sep 2022
Cited by 7 | Viewed by 3004
Abstract
In this review, we discuss the role of liver X receptors (LXRs) in glial cells (microglia, oligodendrocytes and astrocytes) in the central nervous system (CNS). LXRs are oxysterol-activated nuclear receptors that, in adults, regulate genes involved in cholesterol homeostasis, the modulation of inflammatory [...] Read more.
In this review, we discuss the role of liver X receptors (LXRs) in glial cells (microglia, oligodendrocytes and astrocytes) in the central nervous system (CNS). LXRs are oxysterol-activated nuclear receptors that, in adults, regulate genes involved in cholesterol homeostasis, the modulation of inflammatory responses and glutamate homeostasis. The study of LXR knockout mice has revealed that LXRβ plays a key role in maintaining the health of dopaminergic neurons in the substantia nigra, large motor neurons in the spinal cord and retinal ganglion cells in the eye. In the peripheral nervous system (PNS), LXRβ is responsible for the health of the spiral ganglion neurons (SGNs) in the cochlea. In addition, LXRs are essential for the homeostasis of the cerebrospinal fluid (CSF), and in LXRαβ−/− mice, the lateral ventricles are empty and lined with lipid-laden cells. As LXRαβ−/− mice age, lipid vacuoles accumulate in astrocytes surrounding blood vessels. By seven months of age, motor coordination becomes impaired, and there is a loss of motor neurons in the spinal cord of LXRβ−/− mice. During development, migration of neurons in the cortex and cerebellum is retarded in LXRβ−/− mice. Since LXRs are not expressed in dopaminergic or motor neurons in adult mice, the neuroprotective effects of LXRs appear to come from LXRs in glial cells where they are expressed. However, despite the numerous neurological deficits in LXR−/− rodents, multiple sclerosis has the clear distinction of being the only human neurodegenerative disease in which defective LXR signaling has been identified. In this review, we summarize the regulation and functions of LXRs in glial cells and analyze how targeting LXRs in glial cells might, in the future, be used to treat neurodegenerative diseases and, perhaps, disorders caused by aberrant neuronal migration during development. Full article
(This article belongs to the Special Issue Glial Cells Function and Neuron-Glia Crosstalk in Neurological Diseases)
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